Search Results - (Author, Cooperation:W. W. Zhang)
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1Latest Papers from Table of Contents or Articles in PressH. Cao, F. Feng, M. Xun, P. Huang, Y. G. Li, T. Ji, G. Q. Wei, W. W. Zhang, H. Q. Yang
Wiley-Blackwell
Published 2018Staff ViewPublication Date: 2018-01-24Publisher: Wiley-BlackwellPrint ISSN: 1351-0754Electronic ISSN: 1365-2389Topics: GeosciencesAgriculture, Forestry, Horticulture, Fishery, Domestic Science, NutritionPublished by: -
2Latest Papers from Table of Contents or Articles in PressStaff View
Publication Date: 2018-07-31Publisher: Institute of Physics (IOP)Print ISSN: 1755-1307Electronic ISSN: 1755-1315Topics: GeographyGeosciencesPhysicsPublished by: -
3Latest Papers from Table of Contents or Articles in PressS. E. Boggs ; F. A. Harrison ; H. Miyasaka ; B. W. Grefenstette ; A. Zoglauer ; C. L. Fryer ; S. P. Reynolds ; D. M. Alexander ; H. An ; D. Barret ; F. E. Christensen ; W. W. Craig ; K. Forster ; P. Giommi ; C. J. Hailey ; A. Hornstrup ; T. Kitaguchi ; J. E. Koglin ; K. K. Madsen ; P. H. Mao ; K. Mori ; M. Perri ; M. J. Pivovaroff ; S. Puccetti ; V. Rana ; D. Stern ; N. J. Westergaard ; W. W. Zhang
American Association for the Advancement of Science (AAAS)
Published 2015Staff ViewPublication Date: 2015-05-09Publisher: American Association for the Advancement of Science (AAAS)Print ISSN: 0036-8075Electronic ISSN: 1095-9203Topics: BiologyChemistry and PharmacologyComputer ScienceMedicineNatural Sciences in GeneralPhysicsPublished by: -
4Latest Papers from Table of Contents or Articles in PressM. Bachetti ; F. A. Harrison ; D. J. Walton ; B. W. Grefenstette ; D. Chakrabarty ; F. Furst ; D. Barret ; A. Beloborodov ; S. E. Boggs ; F. E. Christensen ; W. W. Craig ; A. C. Fabian ; C. J. Hailey ; A. Hornschemeier ; V. Kaspi ; S. R. Kulkarni ; T. Maccarone ; J. M. Miller ; V. Rana ; D. Stern ; S. P. Tendulkar ; J. Tomsick ; N. A. Webb ; W. W. Zhang
Nature Publishing Group (NPG)
Published 2014Staff ViewPublication Date: 2014-10-10Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsPublished by: -
5Latest Papers from Table of Contents or Articles in PressK. Perez ; C. J. Hailey ; F. E. Bauer ; R. A. Krivonos ; K. Mori ; F. K. Baganoff ; N. M. Barriere ; S. E. Boggs ; F. E. Christensen ; W. W. Craig ; B. W. Grefenstette ; J. E. Grindlay ; F. A. Harrison ; J. Hong ; K. K. Madsen ; M. Nynka ; D. Stern ; J. A. Tomsick ; D. R. Wik ; S. Zhang ; W. W. Zhang ; A. Zoglauer
Nature Publishing Group (NPG)
Published 2015Staff ViewPublication Date: 2015-05-01Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsPublished by: -
6Latest Papers from Table of Contents or Articles in PressG. Risaliti ; F. A. Harrison ; K. K. Madsen ; D. J. Walton ; S. E. Boggs ; F. E. Christensen ; W. W. Craig ; B. W. Grefenstette ; C. J. Hailey ; E. Nardini ; D. Stern ; W. W. Zhang
Nature Publishing Group (NPG)
Published 2013Staff ViewPublication Date: 2013-03-01Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsPublished by: -
7Latest Papers from Table of Contents or Articles in PressB. W. Grefenstette ; F. A. Harrison ; S. E. Boggs ; S. P. Reynolds ; C. L. Fryer ; K. K. Madsen ; D. R. Wik ; A. Zoglauer ; C. I. Ellinger ; D. M. Alexander ; H. An ; D. Barret ; F. E. Christensen ; W. W. Craig ; K. Forster ; P. Giommi ; C. J. Hailey ; A. Hornstrup ; V. M. Kaspi ; T. Kitaguchi ; J. E. Koglin ; P. H. Mao ; H. Miyasaka ; K. Mori ; M. Perri ; M. J. Pivovaroff ; S. Puccetti ; V. Rana ; D. Stern ; N. J. Westergaard ; W. W. Zhang
Nature Publishing Group (NPG)
Published 2014Staff ViewPublication Date: 2014-02-21Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsPublished by: -
8Articles: DFG German National LicensesStaff View
ISSN: 0014-5793Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: BiologyChemistry and PharmacologyPhysicsType of Medium: Electronic ResourceURL: -
9Articles: DFG German National LicensesStaff View
ISSN: 0006-291XSource: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002Topics: BiologyChemistry and PharmacologyPhysicsType of Medium: Electronic ResourceURL: -
10Articles: DFG German National LicensesStaff View
ISSN: 1432-1440Keywords: Antisense ; Oncogene ; Gene therapySource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract Rapid advances in cancer gene therapy are driven by an explosive development of gene transfer technology and a strong demand for seeking alternatives to unsatisfactory conventional cancer therapies. Discovery of the genetic basis of cancer has indicated that cancer is a disease of genes. Among a variety of approaches to gene therapy of cancer, antisense oncogene and tumor suppressor gene therapy of cancer are the two strategies that aim at correcting genetic disorders of cancer through suppression of the abnormal expression of the proliferative genes. The potential effectiveness of these approaches is promised by their precise targeting at the mechanisms of the disease. Examples of several preclinical studies of these types of approaches that led to the approval of clinical trials are reviewed. Limitation and future development of these approaches are also discussed.Type of Medium: Electronic ResourceURL: -
11Articles: DFG German National LicensesStaff View
ISSN: 1432-0533Keywords: Key words Amyloid angiopathy ; Alzheimer’s disease ; Extracellular matrix ; Immunohistochemistry ; MicroangiopathySource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract Cerebral amyloid angiopathies comprise a heterogeneous group of conditions characterised by amyloid deposition in leptomeningeal and cortical vessels. We have studied the deposition of extracellular matrix components in such vessels from controls and ten cases with marked amyloid angiopathy. Arterial vessels which were heavily loaded with amyloid often showed lack of immunostaining to collagen type I, III, V and VI in the amyloid-containing parts of the vessel wall but some immunoreactivity remained in the adventitia. The subintimal region of some arterioles presented a faint staining with collagen V and collagen VI antisera. Immunostaining to collagen IV and laminin revealed normal reactivity in the vascular basal lamina and frequently remaining activity in the media. Immunostaining for actin showed a complete or partial loss of reactivity in the amyloid-containing parts of the media but often there was a thin line of staining at the position of pericytes. The endothelial markers did not reveal any changes compared with controls. In other cerebral microangiopathies, for instance Binswanger’s leukoencephalopathy, CADASIL and cases presenting hyalinosis there is a deposition of fibrillary collagens in the wall of afflicted microvessels. Degeneration of smooth muscle cells and absence of marked fibrosis in some of the arterial vessels in cases of amyloid angiopathy may explain why such vessels are susceptible to ruptures and haemorrhages.Type of Medium: Electronic ResourceURL: -
12Articles: DFG German National LicensesStaff View
ISSN: 1432-0533Keywords: Key words Arteriolosclerosis ; Binswanger’s ; encephalopathy ; Dementia ; Extracellular matrix ; ImmunohistochemistrySource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract A pronounced obliterative microangiopathy of the deep cerebral white matter is one of the cardinal features in classical cases of Binswanger’s encephalopathy. We have characterised the alterations taking place in the intima, media and adventitia of obliterated arterial vessels in seven autopsy cases of this encephalopathy. The adventitia of fibrosed vessels showed immunoreactive material indicating a marked deposition of normally occurring collagen types, i.e. I, III and V. Similar deposits occurred in degenerated parts of the media. Two of the cases had, in addition, signs of collagen type VI-immunoreactive material in the adventitia and media. The elastica of arteries was often split and formed multiple layers. The inner part of the blood vessel walls contained immunoreactivity to collagen type IV and laminin, indicating increased amounts of basal lamina components. Using actin immunostaining the fibrosed arterial vessels showed a severe reduction of smooth muscle cells of the media. However, many terminal arterioles presented a marked actin immunostaining, possibly indicating hypertrophy of smooth muscle cells. The endothelial cell layer did not show any changes with regard to expression of glucose transporter 1, factor VIII, Ulex europaeus agglutinin I and CD34. Degeneration of the media associated with depositions of collagens type I, III, IV, V and possibly type VI, as well as other components of extracellular matrix, will jeopardise the regulatory functions of the afflicted vessels. The maintenance of the endothelial lining of the obliterated vessels probably counteracts thrombosis in the vessels.Type of Medium: Electronic ResourceURL: -
13Articles: DFG German National LicensesStaff View
ISSN: 1432-0614Source: Springer Online Journal Archives 1860-2000Topics: BiologyProcess Engineering, Biotechnology, Nutrition TechnologyNotes: Abstract The operon encoding aspartokinase and aspartate semialdehyde dehydrogenase was cloned and sequenced from rifamycin-SV-producing Amycolatopsis mediterranei U32 previously. In the present work, these two genes were introduced into the auxotrophic Escherichia coli strain CGSC5074 (ask −) and E. coli X6118 (asd −), respectively. The A. mediterranei U32 aspartokinase and aspartate semialdehyde dehydrogenase genes can be functionally expressed in E. coli and the gene products are able to substitute for the E. coli enzymes. Histidine-tagged aspartokinase and aspartate semialdehyde dehydrogenase were partially purified from E. coli cellular extracts and their kinetic characteristics were studied. Both aspartokinase and aspartate semialdehyde dehydrogenase showed typical Michaelis-Menten type substrate saturation patterns. Aspartokinase has K m values of 3.4 mM for aspartate and 2.3 mM for ATP, while aspartate semialdehyde dehydrogenase has K m values of 1.25 mM for dl-aspartate semialdehyde and 0.73 mM for NADP, respectively. Aspartokinase was inhibited by l-threonine, l-lysine, and l-methionine, but not by l-isoleucine and diaminopimelate. Aspartate semialdehyde dehydrogenase was not inhibited by any of the end-product amino acids at a concentration of less than 5 mM. Hill plot analysis suggested that aspartokinase was subject to allosteric control by l-threonine. Repression of both aspartokinase and aspartate semialdehyde dehydrogenase gene transcription in A. mediterranei U32 by l-lysine, l-methionine, l-threonine, and l-isoleucine were found. The network of regulation of aspartokinase and aspartate semialdehyde dehydrogenase in rifamycin SV-producing A. mediterranei U32 is presented.Type of Medium: Electronic ResourceURL: